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Eur J Pharmacol. 2014 Feb 15;725:23-31. doi: 10.1016/j.ejphar.2014.01.010. Epub 2014 Jan 17.

A role for diallyl trisulfide in mitochondrial antioxidative stress contributes to its protective effects against vascular endothelial impairment.

Author information

1
Key Laboratory of Basic Pharmacology in Jiangxi Province, Nanchang University, Nanchang 330006, PR China.
2
Key State Laboratory of Food Science & Technology, Nanchang University, Nanchang 330047, PR China; Key Laboratory of Basic Pharmacology in Jiangxi Province, Nanchang University, Nanchang 330006, PR China.
3
Key State Laboratory of Food Science & Technology, Nanchang University, Nanchang 330047, PR China; Key Laboratory of Basic Pharmacology in Jiangxi Province, Nanchang University, Nanchang 330006, PR China. Electronic address: jxhm56@hotmail.com.
4
Key State Laboratory of Food Science & Technology, Nanchang University, Nanchang 330047, PR China; Key Laboratory of Basic Pharmacology in Jiangxi Province, Nanchang University, Nanchang 330006, PR China. Electronic address: qrhuang@ncu.edu.cn.

Abstract

Persistent hyperglycemia increases a systemic oxidative stress, causing the onset of vascular endothelial dysfunction and atherosclerosis. Diallyl trisulfide (DAT), a natural organosulfur compound in garlic, has been reported to have actions of dilating blood vessels and antibacteria, etc. In this study, models of obese diabetic rat in vivo and high glucose concentration (HG)-induced endothelial cell injury in vitro were used to investigate the protective effects of DAT on vascular endothelial injury and its underlying mechanisms. In the in vivo model, the obese diabetic rats were injected venously with DAT (5.0 mg kg(-1)d(-1)) and Vitamin E (1.0 mg kg(-1)d(-1)) respectively, once daily for 7 consecutive days. In the in vitro model, HG-injured HUVEC were treated with or without DAT (25 µmol L(-1), 50 µmol L(-1), 100 µmol L(-1)) or Vitamin E (25 µmol L(-1)) respectively for 24h. The extents of vascular endothelial injury and protective effects of DAT were evaluated. The results both in vivo and in vitro displayed that DAT-treatment significantly attenuated the endothelial cell impairments. Besides, DAT-treatment markedly decreased the levels of malondialdehyde (MDA) and reactive oxygen species, whereas elevated the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mitochondrium. Moreover, DAT-treatment considerably improved mitochondrial respiration function. Taken together, our results suggest that DAT protects vascular endothelium from HG or hyperglycemia induced-injury by reducing mitochondrial oxidative stress. The findings provide a novel insight for DAT to potentially treat the oxidative stress diseases, i.e., atherosclerosis, diabetes, and neurodegenerative diseases.

KEYWORDS:

Diabetes mellitus; Diallyl trisulfide; Endothelial cells; Oxidative stress

PMID:
24440170
DOI:
10.1016/j.ejphar.2014.01.010
[Indexed for MEDLINE]
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